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Article: Decreased affinity of k-receptor binding during reperfusion following ischaemic preconditioning in the rat heart

TitleDecreased affinity of k-receptor binding during reperfusion following ischaemic preconditioning in the rat heart
Authors
KeywordsCardiac protection
Ischaemic preconditioning
κ-receptor
Issue Date1996
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1996, v. 58 n. 16, p. 1307-1313 How to Cite?
AbstractThe effects of ischaemic preconditioning with three cycles of ischaemia of 3 min and reperfusion of 5 min each cycle on ventricular fibrillation threshold (VFT) and ventricular fibrillation (VF), and binding properties of tritiated U69,593, a selective kappa opioid-receptor (κ-receptor) agonist, during subsequent ischaemia and/or reperfusion were studied in the rat heart. It was found that ischaemic preconditioning significantly enhnaced the VFT values during ischaemia and reperfusion. VF during the subsequent reperfusion period was also significantly reduced. The Kd of the [3H]U69,593 binding sites in the sarcolemma of the heart at 5 min of reperfusion was signficantly increased following ischaemic preconditioning. The Bmax was, however, not altered after the preconditioning. The study provides evidence for the first time suggesting that the cardioprotective effects of ischaemic preconditioning may be related to a reduction in affinity of the κ-receptor binding.
Persistent Identifierhttp://hdl.handle.net/10722/224099
ISSN
2023 Impact Factor: 5.2
2023 SCImago Journal Rankings: 1.257
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXia, Q-
dc.contributor.authorZhang, WM-
dc.contributor.authorShen, YL-
dc.contributor.authorWong, TM-
dc.date.accessioned2016-03-23T08:02:29Z-
dc.date.available2016-03-23T08:02:29Z-
dc.date.issued1996-
dc.identifier.citationLife Sciences, 1996, v. 58 n. 16, p. 1307-1313-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/224099-
dc.description.abstractThe effects of ischaemic preconditioning with three cycles of ischaemia of 3 min and reperfusion of 5 min each cycle on ventricular fibrillation threshold (VFT) and ventricular fibrillation (VF), and binding properties of tritiated U69,593, a selective kappa opioid-receptor (κ-receptor) agonist, during subsequent ischaemia and/or reperfusion were studied in the rat heart. It was found that ischaemic preconditioning significantly enhnaced the VFT values during ischaemia and reperfusion. VF during the subsequent reperfusion period was also significantly reduced. The Kd of the [3H]U69,593 binding sites in the sarcolemma of the heart at 5 min of reperfusion was signficantly increased following ischaemic preconditioning. The Bmax was, however, not altered after the preconditioning. The study provides evidence for the first time suggesting that the cardioprotective effects of ischaemic preconditioning may be related to a reduction in affinity of the κ-receptor binding.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectCardiac protection-
dc.subjectIschaemic preconditioning-
dc.subjectκ-receptor-
dc.subject.meshBenzeneacetamides-
dc.subject.meshMyocardial Ischemia - metabolism - physiopathology-
dc.subject.meshMyocardium - metabolism - ultrastructure-
dc.subject.meshSarcolemma - metabolism - ultrastructure-
dc.subject.meshVentricular Fibrillation - etiology - metabolism-
dc.titleDecreased affinity of k-receptor binding during reperfusion following ischaemic preconditioning in the rat heart-
dc.typeArticle-
dc.identifier.emailWong, TM: wongtakm@hkucc.hku.hk-
dc.identifier.doi10.1016/0024-3205(96)00096-3-
dc.identifier.pmid8614287-
dc.identifier.scopuseid_2-s2.0-0030001778-
dc.identifier.hkuros15427-
dc.identifier.volume58-
dc.identifier.issue16-
dc.identifier.spage1307-
dc.identifier.epage1313-
dc.identifier.isiWOS:A1996UA67500002-
dc.publisher.placeUnited States-
dc.identifier.issnl0024-3205-

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